| Abstrakt: |
Here, we report the genetic features and evolutionary mechanisms of two tet (M)-bearing plasmids (pTA2 and pTA7) recovered from swine Escherichia coli isolates. The genetic profiles of pTA2 and pTA7 and corresponding transconjugants were accessed by S1 nuclease pulsed-field gel electrophoresis and Southern hybridization, followed by whole genome sequencing and bioinformatics analysis. The biological influences of pTA2 and pTA7 were determined by stability and direct competition assays. Both pTA7 and pTA2 had the IncR backbone sequences but differed in the multidrug resistance region (MDR). The MDR of pTA2 consisted of sul3 , tet (M), qnr S1, bleO , oqxAB , floR , aadA1 , cmlA1 , aadA2 , and tet (A)- tetR (A) in addition to 22 insertion sequences. Notably, pTA2 carried the novel complex Tn 7124 (IS 26 -ctp-lp- tet (M)-hp-IS 406 tnp-IntI4-IS 26) harboring tet (M). The fragment carrying tet (M) (IS 26-ctp- lp- tet (M)-IS 406 tnp-ctp-aadA1 - cmlA1 - aadA2 - dfrA12- Int I1), named Tn 6942-like , and the two resistance modules IS Vsa3 - VirD2 - floR - lysR and tet (A)- tetR (A) were located in the MDR of pTA7. Both pTA2 and pTA7 were highly stable in E. coli DH5α cells with no fitness cost to the host or disadvantage in growth competition. These results indicate that transposons carrying tet (M) continuously integrate via mediation with an insertion sequence, which accelerates the transmission of tet (M) in E. coli isolates through integration of other drug-resistant genes, thereby posing a potential serious threat to the efficacy of clinical treatment. [ABSTRACT FROM AUTHOR] |
